Mechanisms of allergySubstance P and its receptor neurokinin 1 expression in asthmatic airways☆,☆☆
Section snippets
Subjects
Twenty-eight subjects were recruited by means of newspaper and radio advertisements from the general community of Denver, Colorado. Eleven of these subjects came from our previous report of M pneumoniae detection by means of PCR,15 and 17 subjects were new to this study. The asthmatic subjects fulfilled criteria for asthma exhibiting a PC20 to methacholine of less than 8 mg/mL and reversibility of lung function by at least 15% with a bronchodilator. Control subjects exhibited no evidence of
Subjects
The characteristics of asthmatic and normal control subjects are shown in Table I.
ICS, Inhaled corticosteroids.Empty Cell Asthmatic subjects (n = 18) Control subjects (n = 10) Sex (M/F) 10/8 6/4 Age (y) 34.0 ± 2.2 30.7 ± 2.4 Duration of asthma (y) 22.9 ± 2.8 — FEV1 (L) 2.4 ± 0.2 4.2 ± 0.3* FEV1 (% predicted) 65.6 ± 4.8 103.8 ± 5.2* PC20 (mg/mL) 0.27 ± 0.06 >18* Medications ICS (n = 5), β-agonist (n = 18) None *P < .01 compared with asthmatic subjects.
Discussion
This study demonstrates that compared with normal control subjects, asthmatic subjects have increased expression of substance P and its receptor neurokinin 1 in the airway epithelium but not in the submucosa. Consistent with this finding, increased mucus production was also observed in asthmatic subjects, and it was inversely correlated with FEV1. The increased epithelial substance P and neurokinin 1 expression in asthmatic subjects appears to be associated with the detection of M pneumoniae in
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2021, European Journal of Pharmaceutical SciencesCitation Excerpt :Upon SP binding, NK-1R initiates signaling cascades to induce transcription factor NF-κb and subsequent proinflammatory cytokines (Williams et al., 2007; Bost, 2004). During viral infection and inflammation, NK-1R is upregulated on the surface of pulmonary epithelial cells and immune cells (Bai et al., 1995; Chu et al., 2000; King et al., 2001). Meanwhile, SP is produced and released into the extracellular space by airway epithelia to escalate the inflammation through autocrine and paracrine signaling (King et al., 2001; Stewart et al., 2008; Suvas, 2017).
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Supported by the American Lung Association-ARC and the National Heart, Lung and Blood Institute (HL 36577).
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Reprint requests: Richard J. Martin, MD, National Jewish Medical and Research Center, 1400 Jackson St, Room J116, Denver, CO 80206.